Pharm (Pages 225-248) Flashcards Preview

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Flashcards in Pharm (Pages 225-248) Deck (155)
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1

α1

G-Protein Class/Major Functions

q

Increase vascular smooth muscle contraction, Increase pupillary dilator muscle contraction (mydriasis), Increase intestinal and bladder sphincter muscle contraction

2

α2

G-Protein Class/Major Functions

i

Decreases sympathetic outflow, Decreases insulin release, Decreases, lipolysis, Decreases platelet aggregation

3

β1

G-Protein Class/Major Functions

s

Increase heart rate, Increase contractility, Increase renin release, Increase lipolysis

4

β2

G-Protein Class/Major Functions

s

Vasodilation, bronchodilation, Increase heart rate, Increase contractility, Increase lipolysis, Increase insulin release, DECREASED uterine tone (tocolysis), ciliary muscle relaxation, q aqueous humor production

5

M1

G-Protein Class/Major Functions

q

CNS, enteric nervous system

6

M2

G-Protein Class/Major Functions

i

Decreased heart rate and contractility of atria

7

M3

G-Protein Class/Major Functions

q

Increased exocrine gland secretions (e.g., lacrimal, salivary, gastric acid), increased gut peristalsis, increased bladder contraction, bronchoconstriction, decreased pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accommodation)

8

D1

G-Protein Class/Major Functions

s

Relaxes renal vascular smooth muscle

9

D2

G-Protein Class/Major Functions

i

Modulates transmitter release, especially in brain

10

H1

G-Protein Class/Major Functions

q

Increases nasal and bronchial mucus production, Increases vascular permeability, contraction of bronchioles, pruritus, and pain

11

H2

G-Protein Class/Major Functions

s

Increases gastric acid secretion

12

V1

G-Protein Class/Major Functions

q

Increases vascular smooth muscle contraction

13

V2

G-Protein Class/Major Functions

s

Increases H2O permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys)

14

Bethanechol

Clinical applications/action

Postoperative ileus, neurogenic ileus, and
urinary retention

Activates bowel and bladder smooth
muscle; resistant to AChE. “Bethany, call
(bethanechol) me, maybe, if you want to
activate your bowels and bladder.”

Direct agonist

15

Carbachol

Clinical applications/action

Glaucoma, pupillary constriction, and relief of
intraocular pressure

Carbon copy of acetylcholine.

Direct agonist

16

Pilocarpine

Clinical applications/action

Potent stimulator of sweat, tears, and saliva
Open-angle and closed-angle glaucoma

Contracts ciliary muscle of eye (open-angle glaucoma), pupillary sphincter (closed-angle glaucoma); resistant to AChE. “You cry, drool, and sweat on your ‘pilow.’ ”

Direct agonist

17

Methacholine

Clinical applications/action

Challenge test for diagnosis of asthma

Stimulates muscarinic receptors in airway when inhaled.

Direct agonist

18

Neostigmine

Clinical applications/action

Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative)

Increases endogenous ACh.
Neo CNS = No CNS penetration.

Indirect agonist

19

Pyridostigmine

Clinical applications/action

Myasthenia gravis (long acting); does not
penetrate CNS

Increases endogenous ACh; increases strength. Pyridostigmine gets rid of myasthenia gravis.

Indirect agonist

20

Physostigmine

Clinical applications/action

Anticholinergic toxicity (crosses blood-brain
barrier to CNS)

Increases endogenous ACh. Physostigmine “phyxes”
atropine overdose.

Indirect agonist

21

Donepezil,
rivastigmine,
galantamine

Clinical applications/action

Alzheimer disease

Increases endogenous ACh.

Indirect agonist

22

Edrophonium

Clinical applications/action

Diagnosis of MG (extremely short acting)
MG is now diagnosed by anti-AChR Ab test

Increases endogenous ACh.

Indirect agonist

23

With all cholinomimetic agents, watch for:

With all cholinomimetic agents, watch for exacerbation of COPD, asthma, and peptic ulcers when giving to susceptible patients.

Indirect agonist

24

Cholinesterase inhibitor poisoning

Antidote:

Often due to organophosphates, such as
parathion, that irreversibly inhibit AChE.
Causes Diarrhea, Urination, Miosis,
Bronchospasm, Bradycardia, Excitation
of skeletal muscle and CNS, Lacrimation,
Sweating, and Salivation.

DUMBBELSS.
Organophosphates are components of
insecticides; poisoning usually seen in farmers.

Antidote—atropine (competitive inhibitor) +
pralidoxime (regenerates AChE if given early).

25

Atropine,
homatropine,
tropicamide

Clinical organ system/applications

Eye

Produce mydriasis and cycloplegia.

Muscarinic antagonist

26

Benztropine

Clinical organ system/applications

CNS

Parkinson disease—“Park my Benz.”

Muscarinic antagonist

27

Scopolamine

Clinical organ system/applications

CNS

Motion sickness.

Muscarinic antagonist

28

Ipratropium,
tiotropium

Clinical organ system/applications

Respiratory

COPD, asthma (“I pray I can breathe soon!”).

Muscarinic antagonist

29

Oxybutynin,
darifenacin, and
solifenacin

Clinical organ system/applications

Genitourinary

Reduce urgency in mild cystitis and reduce
bladder spasms. Other agents: tolterodine,
fesoterodine, trospium.

Muscarinic antagonist

30

Glycopyrrolate

Clinical organ system/applications

Gastrointestinal, respiratory

Parenteral: preoperative use to reduce airway secretions.
Oral: drooling, peptic ulcer.

Muscarinic antagonist